Molecular mimicry to Borrelia burgdorferi: pathway to autoimmunity?

• Published in: Autoimmunity (Chur, Switzerland) Vol. 37; no. 5; pp. 387 - 392
• Main Authors: Bolz, Devin D, Weis, Janis J
• Format: Journal Article
• Language: English
• Published: England 01.08.2004
• Subjects: Antigens, Surface - genetics; Antigens, Surface - immunology; Autoimmunity - immunology; Bacterial Outer Membrane Proteins - genetics; Bacterial Outer Membrane Proteins - immunology; Bacterial Vaccines; Borrelia burgdorferi; Borrelia burgdorferi - immunology; Chronic Disease; Humans; Lipoproteins - genetics; Lipoproteins - immunology; Lyme Disease - immunology; Lymphocyte Function-Associated Antigen-1 - genetics; Lymphocyte Function-Associated Antigen-1 - immunology; Molecular Mimicry - genetics; Molecular Mimicry - immunology; Spirochetes; T-Lymphocytes - immunology
• ISSN: 0891-6934; 1607-842X
• DOI: 10.1080/08916930410001713098

Lyme borreliosis is due to infection with the tick-borne spirochete Borrelia burgdorferi, and is associated with persistent infection unless treated with antibiotics. The persistent nature of infection by B. burgdorferi can lead to development of chronic disease, as found in patients infected before recognition of the effectiveness of antibiotic therapy. Much speculation has surrounded the possibility that autoimmune mechanisms are involved in chronic symptoms. In most cases, involvement of autoimmunity in Lyme disease has not received experimental support. The exception is in a small group of patients with chronic arthritis whose abnormal joint symptoms persist after apparent elimination of the bacteria. In this review, the evidence supporting autoimmune mechanisms in Lyme disease will be discussed.